The proposed experiments examine how the N-methyl-D-aspartate receptor channel is regulated by an activity dependent mechanism, which undergoes a major subunit switch, and a pronounced functional down-regulation just as map refinement is complete. In addition, we plan to investigate the effects on chronically stimulating the NMDA receptor in the developing superior colliculus. Preliminary data suggests that this treatment abnormally increases inhibition and results in circuit induced suppression of the NMDA receptor function. Since the NMDA receptor is a major calcium gate for young neurons, we propose that down regulation and suppression of the NMDA receptor has evolved to control the receptors function in order to maintain calcium homeostasis. I will investigate whether the normal developmental, and experimentally induced changes in NMDA function in the superior colliculus are paralleled by changes in calcium permeability of the cell, and if these changes are due to changes in circuitry or are pre-programmed. Finally, I will determine if inhibition after chronic NMDA treatment make pronounced changes in calcium flux through the NMDA channel.